Anestesiologia

Dysphagia after stroke is common, especially in severely affected patients who have had a tracheotomy. In a pilot trial, pharyngeal electrical stimulation (PES) improved swallowing function in this group of patients. We aimed to replicate and extend this single-centre experience.

Methods

We did a prospective, single-blind, randomised controlled trial across nine sites (seven acute care hospitals, two rehabilitation facilities) in Germany, Austria, and Italy. Patients with recent stroke who required tracheotomy were randomly assigned to receive 3 days of either PES or sham treatment (1:1). All patients had the stimulation catheter inserted; sham treatment was applied by connecting the PES base station to a simulator box instead of the catheter. Randomisation was done via a computerised interactive system (stratified by site) in blocks of four patients per site. Patients and investigators applying PES were not masked. The primary endpoint was assessed by a separate investigator at each site who was masked to treatment assignment. The primary outcome was readiness for decannulation 24–72 h after treatment, assessed using fibreoptic endoscopic evaluation of swallowing and based on a standardised protocol, including absence of massive pooling of saliva, presence of one or more spontaneous swallows, and presence of at least minimum laryngeal sensation. We planned a sequential statistical analysis of superiority for the primary endpoint. Interim analyses were to be done after primary outcome data were available for 50 patients (futility), 70 patients, and every additional ten patients thereafter, up to 140 patients. Analysis was by intention to treat. This trial is registered with the ISRCTN registry, number ISRCTN18137204.

Findings

From May 29, 2015, to July 5, 2017, of 81 patients assessed, 69 patients from nine sites were randomly assigned to receive PES (n=35) or sham (n=34) treatment. Median onset to randomisation time was 28 days (IQR 19–41; PES 28 [20–49]; sham 28 [18–40]). The Independent Data and Safety Monitoring Board recommended that the trial was stopped early for efficacy after 70 patients had been recruited and primary endpoint data for 69 patients were available. This decision was approved by the steering committee. More patients were ready for decannulation in the PES group (17 [49%] of 35 patients) than in the sham group (three [9%] of 34 patients; odds ratio [OR] 7.00 [95% CI 2.41–19.88]; p=0.0008). Adverse events were reported in 24 (69%) patients in the PES group and 24 (71%) patients in the sham group. The number of patients with at least one serious adverse event did not differ between the groups (ten [29%] patients in the PES group vs eight [23%] patients in the sham group; OR 1.30 [0.44–3.83]; p=0.7851). Seven (20%) patients in the PES group and three (9%) patients in the sham group died during the study period (OR 2.58 [0.61–10.97]; p=0.3059). None of the deaths or serious adverse events were judged to be related to PES.

Interpretation

In patients with stroke and subsequent tracheotomy, PES increased the proportion of patients who were ready for decannulation in this study population, many of whom received PES within a month of their stroke. Future trials should confirm whether PES is beneficial in tracheotomised patients who receive stimulation similarly early after stroke and explore its effects in other cohorts.

Among the presentations at the 2018 Euroanaesthesia congress in Denmark last week, was a case report of a patient who remained conscious and aware during resuscitation following a cardiac arrest.

Presenter, Dr Rune Lundsgaard from the Department of Anaestesiology at Herlev Hospital in Copenhagen and Nykøbing Falster Hospital, Denmark, said the scenario raises ethical questions about proper sedation during resuscitation, which is not currently part of guidelines.

The 69-year old male patient was admitted to the hospital after three days of dyspeptic symptoms. During admission a short period of tachycardia was followed by asystolic cardiac arrest. CPR was immediately initiated.

Throughout the arrest, the patient retained a high level of awareness, with open eyes and movement of the head and limbs. After three minutes of asystole, epinephrine was administered in 1mg boluses every 3-5 minutes. By the third hands-off for rhythm evaluation, the patient was orally intubated but there was still a high level of awareness. Despite 90 minutes of CPR, the patient did not survive. Autopsy later reported a complete aortic dissection.

Dr Lundsgaard said that even though the prognosis was poor, the termination of CPR raised ethical questions for the team as the patient was still conscious at the time.

New research suggests droperidol is superior to midazolam for the prehospital management of acute behavioural disturbance.

With backing from the Emergency Medicine Foundation (EMF) Australasia, the Queensland Ambulance Service (QAS) in Australia has conducted the world’s first comparison of midazolam with droperidol in a prehospital setting. The study revealed that droperidol was associated with fewer adverse events, a shorter time to sedation, and fewer requirements for additional sedation.

In 2016, the QAS introduced droperidol as one of several initiatives to reduce escalating violence against paramedics. This new prospective study compared patient outcomes before and after the introduction of droperidol.

The data showed fewer adverse events with droperidol compared to midazolam (7% vs. 23%; absolute difference 16%; 95% CI 8-24%; P=.0001). Median time to sedation was 22 minutes with droperidol versus 30 minutes with midazolam. Additional prehospital sedation was required in 4 per cent of droperidol patients and 14 per cent of midazolam patients. Approximately 7 per cent of droperidol and 42 per cent of midazolam patients required further sedation in the emergency department. However, there were no differences in patient or staff injuries.

The authors predict that droperidol will now become extensively embedded in ambulance services around the world.

While atraumatic needles have been proposed to lower complication rates following lumbar puncture, several surveys show that clinical adoption of these needles remains limited. Findings from a new study however suggest using atraumatic needles rather than conventional traumatic needles for lumbar punctures is not only as effective, but results in a significant decrease in complications.

As part of a new study, published in The Lancet , researchers undertook a systematic review and meta-analysis of randomised controlled trials with more than 30,000 participants in 28 countries, comparing atraumatic and conventional needles.

They found the incidence of post-dural puncture headache was significantly reduced from 11 per cent in the conventional needle group to 4.2 per cent in the atraumatic group. The need for intravenous fluid or controlled analgesia was lower with atraumatic needles (2.2 per cent vs 4.5 per cent) as was the requirement for epidural blood patch (1.1 per cent vs 3.0 per cent). Rates of failure and success on first attempt were similar for both needle types.

Writing in a linked commentary, Diederik van de Beek and Matthijs Brouwer, of the University of Amsterdam recommend clinicians “change practice” and begin using atraumatic needles for lumbar punctures.

Living Art Enterprises / Science Source
It used to be said that missing the clinical diagnosis of aortic dissection was “the standard” as it is rare and often presents atypically. The diagnosis rate of aortic dissection changed with the landmark International Registry of Acute Aortic Dissection (IRAD) study in 2000, which deepened our understanding of the presentation.1 Nonetheless, aortic dissection remains difficult to diagnose, with one in six missed at the initial ED visit.

Herein lies the difficulty. Aortic dissection must be considered in all patients with chest, abdominal, or back pain; syncope; or stroke symptoms. Yet, we shouldn’t be working up every one of them, creating a resource utilization disaster. However, early, timely diagnosis is essential because each hour that passes from the onset of symptoms correlates with a 1 percent to 2 percent increase in mortality.

In this column, I’ll elucidate how to improve your diagnosis rate, without overimaging, by explaining five pain pearls, the concepts of “CP +1” and “1+ CP,” physical exam nuances, and how best to initially utilize tests.

The Five Pain Pearls of Aortic Dissection

Ask the following three things of all patients with torso pain:
What is the quality of pain? (The pain from aortic dissection is most commonly described as “sharp,” but the highest positive likelihood ratio [+LR] is for “tearing.”)
What was the pain intensity at onset? (It is abrupt in aortic dissection.)
What is the radiation of pain? (It is in the back and/or abdomen in aortic dissection.)
A 1998 study that reviewed a series of aortic dissection cases showed that for the 42 percent of physicians who asked about these three things, the diagnosis was suspected in 91 percent. When fewer than three questions were asked, dissection was suspected in only 49 percent.2

Think of aortic dissection as the subarachnoid hemorrhage of the torso. Just like a patient who presents with a new-onset, severe, abrupt headache should be suspected of having a subarachnoid hemorrhage, if a patient describes a truly abrupt onset of severe torso pain with maximal intensity at onset, think aortic dissection.
If you find yourself treating your chest pain patient with IV opioids to control severe colicky pain, think about aortic dissection.
Migrating pain has a +LR of 7.6.1 In addition to the old adage, “Pain above and below the diaphragm should heighten your suspicion for aortic dissection,” severe pain that progresses and moves in the same vector as the aorta significantly increases the likelihood of aortic dissection.
The pain can be intermittent as dissection of the aortic intima stops and starts. The combination of severe migrating and intermittent pain should raise the suspicion for aortic dissection.
Painless Aortic Dissection

While IRAD reported a painless aortic dissection rate of about 5 percent, a more recent study out of Japan reported that 17 percent of aortic dissection patients had no pain.3 These patients presented more frequently with a persistent disturbance of consciousness, syncope, or a focal neurological deficit. Cardiac tamponade was more frequent in the pain-free group as well.

The Concepts of “CP +1” and “1+ CP”

The intimal tear in the aorta can devascularize any organ from head to toe, including the brain, heart, kidneys, and spinal cord. Thus, 5 percent of dissections present as strokes, and these certainly are not the kind of stroke patients who should be receiving tPA! An objective focal neurologic deficit in the setting of acute, unexplained chest pain (CP) has +LR of 33 for aortic dissection, almost diagnostic. Some of the CP +1 phenomena to think about include torso pain, cerebrovascular accident, paralysis, hoarseness (recurrent laryngeal nerve), and limb ischemia.

(click for larger image) These three coronal reconstructions from contrast enhanced CT angiograms of the chest show an extensive dissection of the thoracic aorta. This is a De Bakey type I or Standord A aortic dissection.
Source: Living Art Enterprises / Science Source
In addition to thinking of CP +1, it may help to think backwards in time (1+ CP) and ask patients who present with end-organ damage if they had torso pain prior to their symptoms of end organ damage. For example, ask patients who present with stroke symptoms if they had torso pain before the stroke symptoms.

Anyone under the age of 40 years who presents to the emergency department with unexplained torso pain should be asked if they have Marfan syndrome. In the IRAD analysis of those under 40 years, 50 percent of the aortic dissection patients had Marfan syndrome, representing 5 percent of all dissections.1

Look. The patient doesn’t always know they have Marfan syndrome, so you need to look for arachnodactyly (elongated fingers), pectus excavatum (sternal excavation), and lanky limbs.
Listen. A new aortic regurgitation murmur has a surprisingly high +LR of 5.
Feel. Feel for a pulse deficit, which has a +LR of 2.7, much higher than that of interarm blood pressure differences.
The patient’s blood pressure needs to be interpreted with caution and insight. Do not assume that the patient with a normal or low blood pressure does not have an aortic dissection. We know from the IRAD data that only about half of patients are hypertensive at initial presentation. Patients with aortic dissections that progress into the pericardium, resulting in cardiac tamponade, are often hypotensive. Patients with dissection who have a wide pulse pressure should be considered preterminal and usually require immediate surgery.

There is a lot more to chest radiograph interpretation for suspected aortic dissection than looking for a wide mediastinum. One-third of chest radiographs in aortic dissection are normal to the untrained eye, and a common pitfall is to assume that if the chest X-ray is normal, the patient does not have an aortic dissection. There are about a dozen X-ray findings associated with dissection, but two of them are especially important: loss of the aortic knob/aortopulmonary window and the calcium sign.

Look for a white line of calcium within the aortic knob, then measure the distance from there to the outer edge of the aortic knob. A distance >0.5 cm is considered a positive calcium sign, and a distance >1.0 cm is considered highly suspicious for aortic dissection. It is always wise to compare to an old film to see if there’s been an interval change.

Eighteen percent of patients with aortic dissection will have a positive troponin test, so if you suspect the diagnosis based on other clinical findings, don’t assume isolated acute coronary syndrome when the troponin comes back positive.5 Remember that fewer than one in 100 patients with a dissection will have associated coronary ischemia in any coronary distribution (most commonly inferior).

While D-dimer seems like it might be appealing to help rule out the diagnosis in low-risk patients, for such a rare diagnosis and poor test characteristics of D-dimer for dissection, guidelines do not recommend the use of D-dimer for the workup of aortic dissection.6

Aortic dissection can be considered the retinal detachment of the torso. While the sensitivity of point-of-care ultrasound (POCUS) by emergency physicians to detect an intimal flap is only 67 percent, the specificity has been shown to be 99 percent to 100 percent.7 For patients suspected of the diagnosis, look for an intimal flap that looks similar to a retinal detachment on POCUS and look for a pericardial effusion indicative of a retrograde dissection into the pericardium.8

Take-Home Points

Remember the big pain pearls when taking a history:
Ask the three important questions.
Aortic dissection should be considered the subarachnoid hemorrhage of the torso.
Migrating pain, colicky pain, plus need for IV opioids should raise your suspicion.
Intermittent pain can still be a dissection.
Look for Marfan syndrome, listen for an aortic regurgitation murmur, and feel for a pulse deficit.
Think not only about CP +1 but also 1+ CP.
Know the radiographic findings of loss or aortic knob/aortopulmonary window and the calcium sign, and use POCUS to look for an intimal flap and pericardial effusion.
Don’t be misled by a troponin or D-dimer.
Thanks to David Carr for his expert contributions to the EM Cases podcast that inspired this article.